This study clearly shows that in primates, memory B cells and CD8α+ T cells do not contribute to the control of virus replication after re-challenge with a homologous H1N1 strain of influenza A. In future studies, administration of anti-CD8α, anti-CD4 or anti-CD20 depleting antibodies in rhesus macaques challenged with antigenically-drifted and heterosubtypic influenza A viruses could be used to define the nature of protective, vaccine-induced, and infection-induced immune responses to progressively divergent viruses. The gene discussed is CD8A; the disease is infection.